title: Ang-(1-7) might prevent the development of monocrotaline induced pulmonary arterial hypertension in rats.
abstract: OBJECTIVE
  To investigate whether Angiotensin-(1-7) [Ang-(1-7)] could prevent the development of monocrotaline (MCT) induced pulmonary arterial hypertension and vascular remodeling.
  
  
  METHODS
  30 Sprgue-Dawely rats were randomly assigned into three groups: control group, pulmonary arterial hypertension (PAH) group and PAH +Ang-(1-7) group. Rats in PAH group and PAH +Ang-(1-7) group received 60 mg/kg monocrotaline (MCT) injection subcutaneously and after 24 hours received either saline or 24 microg/kg/h of Ang-(1-7) injection via osmotic minipumps for 4 weeks. Those rats in control group were firstly injected saline subcutaneously and then received saline injection via osmotic minipumps.
  
  
  RESULTS
  After four weeks, in PAH group, right ventricular systolic pressure (RVSP), right ventricular hypertrophy index (RVHI), percentage of wall thickness (WT%) and percentage of wall area (WA%) were significantly increased, and the level of endothelial nitric oxide synthase (eNOS) protein, eNOS ser 1177-phosphorylati, Akt-phosphorylation were significantly decreased compared with control group. However, RVSP, RVHI, WT%, WA% were dramatically decreased in PAH+Ang-(1-7) group and the level of eNOS protein, eNOS ser 1177-phosphorylation, Akt-phosphorylation were significantly increased compared with PAH group.
  
  
  CONCLUSIONS
  Those results suggest that Ang-(1-7) could prevent the development of monocrotaline induced pulmonary arterial hypertension and vascular remodeling, which appears to be associated with up-regulation of eNOS activation via Akt pathway.
authors.affiliation: Division of Cardiology, First Affilliated Hospital Of Kunming Medical College, Cardiovascular Research Institute, Xichang Road 295#, Kunming, China.
authors.forename: L
authors.initials: L
authors.lastname: Chen
authors.forename: J
authors.initials: J
authors.lastname: Xiao
authors.forename: Y
authors.initials: Y
authors.lastname: Li
authors.forename: H
authors.initials: H
authors.lastname: Ma
mesh_terms: D000803:Angiotensin I / Q000627:therapeutic use*; D000818:Animals; D065627:Familial Primary Pulmonary Hypertension; D006439:Hemodynamics / Q000187:drug effects; D006976:Hypertension, Pulmonary / Q000139:chemically induced / Q000503:physiopathology / Q000517:prevention & control; D008297:Male; D016686:Monocrotaline; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D010446:Peptide Fragments / Q000627:therapeutic use*; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D010446:Peptide Fragments; D016686:Monocrotaline; D000803:Angiotensin I; D052250:Nitric Oxide Synthase Type III; D051057:Proto-Oncogene Proteins c-akt; C118790:angiotensin I (1-7)